MicroRNA (miRNA or miR) expression profiles are altered in tissues under hypoxic-ischemic conditions. The expression of miR‑140 is downregulated >2-fold following hypoxic-ischemic brain damage, however, its role in angiogenesis subsequent to cerebral ischemia is not fully understood. The present study aimed to investigate the role of miR-140-5p in angiogenesis and the molecular mechanism mediated by vascular endothelial growth factor A (VEGFA) in an in vitro model for brain ischemia. A rat middle cerebral artery occlusion (MCAO) model was constructed, and the results from reverse transcription-quantitative polymerase chain reaction and western blot analysis demonstrated that the expression levels of miR-140‑5p were significantly decreased, while the expression levels of VEGFA were significantly increased between 12 and 48 h in the rat cerebral following MCAO. Furthermore, human umbilical vein endothelial cells (HUVECs) were exposed to low oxygen conditions and it was demonstrated that hypoxia downregulated miR-140-5p and upregulated VEGFA expression levels. The miR-140-5p mimic was transfected into the normoxic and hypoxic HUVECs and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, Transwell migration and tube formation assays were performed. The results indicated that miR‑140‑5p inhibited angiogenesis by decreasing cell proliferation, migration and tube formation. Additionally, in human embryonic kidney 293 cells, results from the luciferase reporter assay revealed that miR‑140‑5p directly targeted the 3' untranslated region of VEGFA and that miR‑140‑5p regulated the protein expression of VEGFA. To further analyze this effect, a VEGFA‑pEGFP‑C1 plasmid was transfected into the normoxic and hypoxic HUVECs, and it was revealed that the inhibitory effect of miR‑140‑5p on angiogenesis was attenuated by the overexpression of VEGFA. In conclusion, to the best of our knowledge, the present study is the first to suggest that miR‑140‑5p exerts an inhibitory effect on angiogenesis in an in vitro model of ischemia, and this effect is achieved partially by targeting VEGFA. The present study provided a novel biomarker for the treatment of cerebral ischemia.

Many studies have reported the recovery ability of umbilical cord-derived mesenchymal stem cells (UC-MSCs) for neural diseases. In this study, the authors explored the roles of UC-MSCs to treat the traumatic brain injury. Umbilical cord-derived mesenchymal stem cells were isolated from healthy neonatal rat umbilical cord immediately after delivery. The traumatic brain injury (TBI) model was formed by the classical gravity method. The authors detected the behavior changes and measured the levels of inflammatory factors, such as interleukin-lβ and tumor necrosis factor-α by enzyme linked immunosorbent assay (ELISA) at 1, 2, 3, 4 weeks after transplantation between TBI treated and untreated with UC-MSCs. Simultaneously, the expression of glial cell line-derived neurotrophic factor (GDNF) and brain derived neurotrophic factor (BDNF) were measured by real-time–polymerase chain reaction and ELISA.The authors found that the group of transplantation UC-MSCs has a significant improvement than other group treated by phosphate buffered saline. In the behavioral test, the Neurological Severity Scores of UC-MSCs + TBI group were lower than TBI group (P < 0.05), but not obviously higher than control group at 2, 3, and 4week, respectively. The inflammatory factors are significantly reduced comparison with TBI group (P < 0.05), but both GDNF and BDNF were higher than TBI group (P < 0.05). The results indicated that UC-MSCs might play an important role in TBI recovery through inhibiting the release of inflammatory factors and increasing the expression of GDNF and BDNF.

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Heat Shock Protein BAP1 (heat shock 27-kDa-associated protein 1, HSPBAP1) inhibits the function of heat shock protein 27, which has a neuroprotective effect during experimentally induced epileptic neuropathology. In our study, fluorescence quantitative polymerase chain reaction, immunohistochemistry, immunofluorescence, western blot were used to test the levels of HSPBAP1 mRNA and protein in surgical samples of the anterior temporal neocortex of patients with intractable epilepsy (IE) and normal controls samples. HSPBAP1 mRNA was abnormally expressed in the anterior temporal neocortex of patients with IE. Moreover, HSPBAP1 was found extensively in the cytoplasm of neurons and glial cells in all epilepsy specimens. Western blot showed a clear immunoreactive band of HSPBAP1 in IE specimens whereas it was absent in control specimens. The expression of HSPBAP1 mRNA and protein in the anterior temporal neocortex from patients with IE may play a role in the development of epileptic seizures in patients with cell loss in this brain region. Additional studies will be required to elucidate the mechanism by which HSPBAP1 affects brain function in IE.

MicroRNAs (miRNAs) function as potential novel biomarkers for disease detection due to their marked stability in the blood and the characteristics of their expression profile in several diseases. In the present study, microarray‑based serum miRNA profiling was performed on serum obtained from three patients with epilepsy at diagnosis and from three healthy individuals as controls. This was followed by reverse transcription‑quantitative polymerase chain reaction analysis in a separate cohort of 35 health volunteers and 90 patients with epilepsy. The correlations between miRNAs and clinical parameters were analyzed. The array results showed that 15 miRNAs were overexpressed and 10 miRNAs were underexpressed (>2‑fold) in the patients with epilepsy. In addition, four miRNAs, including miR‑30a, miR‑378, miR‑106b and miR‑15a were found to be overexpressed in the serum of patients at seizure onset, compared with post‑seizure. When the patients were at seizure onset, the expression of miR‑30a was positively associated with seizure frequency. No significant differences were found between miR‑30a and gender, age or number of years following diagnosis. The expression levels of miR‑378, miR‑106b and mir‑15a were not associated with the clinical parameters in the patients with seizures. Calcium/calmodulin‑dependent protein kinase type IV was a target of miR‑30a, and its expression was increased following seizure and was negatively correlated with miR‑30a in the patients with epilepsy. The present study provided the first evidence, to the best of our knowledge, that the expression levels of miR‑378, miR‑30a, miR‑106b and miR‑15a were enhanced in epileptic patients with seizures. miR-30a may be useful for prognostic prediction in epilepsy.

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